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Endoscopy Jan 2017This Executive summary of the Guideline on pediatric gastrointestinal endoscopy from the European Society of Gastrointestinal Endoscopy (ESGE) and the European Society...
Pediatric gastrointestinal endoscopy: European Society of Gastrointestinal Endoscopy (ESGE) and European Society for Paediatric Gastroenterology Hepatology and Nutrition (ESPGHAN) Guideline Executive summary.
This Executive summary of the Guideline on pediatric gastrointestinal endoscopy from the European Society of Gastrointestinal Endoscopy (ESGE) and the European Society for Paediatric Gastroenterology Hepatology and Nutrition (ESPGHAN) refers to infants, children, and adolescents aged 0 - 18 years. The areas covered include: indications for diagnostic and therapeutic esophagogastroduodenoscopy and ileocolonoscopy; endoscopy for foreign body ingestion; endoscopic management of corrosive ingestion and stricture/stenosis; upper and lower gastrointestinal bleeding; endoscopic retrograde cholangiopancreatography, and endoscopic ultrasonography. Percutaneous endoscopic gastrostomy and endoscopy specific to inflammatory bowel disease (IBD) have been dealt with in other Guidelines and are therefore not mentioned in this Guideline. Training and ongoing skill maintenance will be addressed in an imminent sister publication.
Topics: Adolescent; Burns, Chemical; Caustics; Child; Child, Preschool; Cholangiopancreatography, Endoscopic Retrograde; Digestive System Diseases; Endoscopy, Gastrointestinal; Endosonography; Foreign Bodies; Gastrointestinal Tract; Humans; Infant; Infant, Newborn
PubMed: 27617420
DOI: 10.1055/s-0042-111002 -
Surgical Case Reports Sep 2021Severe electrical burns are a rare cause of admission to major burn centers. Incidence of electrical injury causing full-thickness injury to viscera is an increasingly...
BACKGROUND
Severe electrical burns are a rare cause of admission to major burn centers. Incidence of electrical injury causing full-thickness injury to viscera is an increasingly scarce, but severe presentation requiring rapid intervention. We report one of few cases of a patient with full-thickness electrical injury to the abdominal wall, bowel, and bladder.
CASE REPORT
The patient, a 22-year-old male, was transferred to our institution from his local hospital after sustaining a suspected electrical burn. On arrival the patient was noted to have severe burn injuries to the lower abdominal wall with evisceration of multiple loops of burned small bowel as well as burns to the groin, left upper, and bilateral lower extremities. In the trauma bay, primary and secondary surveys were completed, and the patient was taken for CT imaging and then emergently to the operating room. On exploration, the patient had massive full-thickness burns to the lower abdominal wall, five full-thickness burns to small bowel, and intraperitoneal bladder rupture secondary to full-thickness burn. The patient underwent damage-control laparotomy including enterectomies, debridement of bladder coagulative necrosis, and layered closure of bladder injury followed by temporary abdominal closure with vacuum dressing. The patient also underwent right leg escharotomy and partial right foot fasciotomies. The patient was subsequently transferred to the nearest burn center for continued resuscitation and comprehensive burn care.
CONCLUSION
Severe electrical burns can be associated with devastating visceral injuries in rare cases. Though uncommon, these injuries are associated with very high mortality rates. The authors assert that rapid evaluation and initial stabilization following ATLS guidelines, damage-control laparotomy, and goal-directed resuscitation in concert with transfer to a major burn center are essential in effecting a successful outcome in these challenging cases.
PubMed: 34585274
DOI: 10.1186/s40792-021-01302-8 -
Neurogastroenterology and Motility Oct 2022The vagus nerve (VN), the longest nerve of the organism innervating the gastrointestinal tract, is a mixed nerve with anti-inflammatory properties through its afferents,... (Review)
Review
The vagus nerve (VN), the longest nerve of the organism innervating the gastrointestinal tract, is a mixed nerve with anti-inflammatory properties through its afferents, activating the hypothalamic-pituitary adrenal axis, and its efferents through the cholinergic anti-inflammatory pathway inhibiting the release of pro-inflammatory cytokines (e.g., TNFα) by splenic and gut macrophages. In addition, the VN is also able to modulate the permeability of the intestinal barrier although the VN does not innervate directly the intestinal epithelium. Targeting the VN through VN stimulation (VNS) has been developed in experimental model of intestinal inflammation and in inflammatory bowel disease (IBD) and might be of interest to decrease intestinal permeability in gastrointestinal disorders with intestinal barrier defect such as IBD, irritable bowel syndrome (IBS), and celiac disease. In this issue of neurogastroenterology and motility, Mogilevski et al. report that a brief non-invasive transcutaneous auricular VNS in healthy volunteers consistently reduces the permeability of the small intestine induced by intravenous administration of the stress peptide corticotropin releasing hormone, known to increase intestinal permeability and to inhibit the VN. In this review, we outline the mechanistic underpinning the effect of stress, of the VN and VNS on intestinal permeability. In particular, the VN can act on intestinal permeability through enteric nerves, and/or cells such as enteric glial cells. We also review the existing evidence of the effects VNS on intestinal permeability in models such as burn intestinal injury and traumatic brain injury, which pave the way for future clinical trials in IBD, IBS, and celiac disease.
Topics: Burns; Celiac Disease; Corticotropin-Releasing Hormone; Cytokines; Humans; Inflammatory Bowel Diseases; Irritable Bowel Syndrome; Tumor Necrosis Factor-alpha; Vagus Nerve; Vagus Nerve Stimulation
PubMed: 36097404
DOI: 10.1111/nmo.14456 -
Shock (Augusta, Ga.) Jun 2015Traumatic injury remains one of the most prevalent reasons for patients to be hospitalized. Burn injury accounts for 40,000 hospitalizations in the United States... (Review)
Review
Traumatic injury remains one of the most prevalent reasons for patients to be hospitalized. Burn injury accounts for 40,000 hospitalizations in the United States annually, resulting in a large burden on both the health and economic system and costing millions of dollars every year. The complications associated with postburn care can quickly cause life-threatening conditions including sepsis and multiple organ dysfunction and failure. In addition, alcohol intoxication at the time of burn injury has been shown to exacerbate these problems. One of the biggest reasons for the onset of these complications is the global suppression of the host immune system and increased susceptibility to infection. It has been hypothesized that infections after burn and other traumatic injury may stem from pathogenic bacteria from within the host's gastrointestinal tract. The intestine is the major reservoir of bacteria within the host, and many studies have demonstrated perturbations of the intestinal barrier after burn injury. This article reviews the findings of these studies as they pertain to changes in the intestinal immune system after alcohol and burn injury.
Topics: Alcoholic Intoxication; Animals; Burns; Homeostasis; Humans; Intestinal Mucosa; Intestines
PubMed: 25692258
DOI: 10.1097/SHK.0000000000000353 -
Biological Trace Element Research Nov 2019Selenium is an essential dietary micronutrient. Ingested selenium is absorbed by the intestines and transported to the liver where it is mostly metabolized to... (Review)
Review
Selenium is an essential dietary micronutrient. Ingested selenium is absorbed by the intestines and transported to the liver where it is mostly metabolized to selenocysteine (Sec). Sec is then incorporated into selenoproteins, including selenoprotein P (SELENOP), which is secreted into plasma and serves as a source of selenium to other tissues of the body. Herein, we provide an overview of the biology of selenium from its absorption and distribution to selenoprotein uptake and degradation, with a particular focus on the latter. Molecular mechanisms of selenoprotein degradation include the lysosome-mediated pathway for SELENOP and endoplasmic reticulum-mediated degradation of selenoproteins via ubiquitin-activated proteasomal pathways. Ubiquitin-activated pathways targeting full-length selenoproteins include the peroxisome proliferator-activated receptor gamma-dependent pathway and substrate-dependent ubiquitination. An alternate mechanism is utilized for truncated selenoproteins, in which cullin-RING E3 ubiquitin ligase 2 targets the defective proteins for ubiquitin-proteasomal degradation. Selenoproteins, particularly SELENOP, may have their Sec residues reutilized for new selenoprotein synthesis via Sec decomposition. This review will explore these aspects in selenium biology, providing insights to knowledge gaps that remain to be uncovered.
Topics: Animals; Humans; Intestinal Mucosa; Liver; Proteasome Endopeptidase Complex; Proteolysis; Selenium; Selenoprotein P
PubMed: 31222623
DOI: 10.1007/s12011-019-01771-x